#223      31 min 50 sec
Mild to severe: What's behind the rise in food allergies in children?

Childhood allergy expert Prof Katie Allen discusses the emerging epidemic of food allergies in children and its causes. Presented by Dr Shane Huntington.

"Where I think the big movement forward will come from genetic technology is stratifying risk by genetic predisposition so that there may be some people who have a more sensitive genetic predisposition that makes them more likely to do poorly to that environmental risk factor." -- Prof Katie Allen




Prof Katie Allen
Prof Katie Allen

Professor Katie Allen is Director of the Population Health, Genes and Environment Research Theme at the Murdoch Childrens Research Institute which comprises 350 researchers.
 
She is also a paediatric gastroenterologist and allergist undertaking research in the evolving field of food allergy and is a prestigious Viertel Senior Medical Research Fellow (worth $1 million). She  is the principal investigator of the HealthNuts study - the largest single centre population-based study of food allergy in children ever mounted which is following 5300 Melbourne infants from birth to age 6 years.
 
Katie has published more than 120 peer-reviewed papers and has recently co-authored the book, Kids Food Allergies for Dummies. She currently supervises 10 PhD students within her research group  and is  a member of various national and international committees including the Scientific Council for Research and Clinical Issues of the World Allergy Organisation.

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Host: Dr Shane Huntington
Producers: Eric van Bemmel, Kelvin Param
Associate Producer: Dr Dyani Lewis
Audio Engineer: Gavin Nebauer
Voiceover: Nerissa Hannink
Series Creators: Kelvin Param & Eric van Bemmel

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VOICEOVER Welcome to Up Close, the research talk show from the University of Melbourne, Australia. 

SHANE HUNTINGTON I’m Shane Huntington. Thanks for joining us. Food allergies from mild to life threatening affect more children today than ever, and this has led to greater and more urgent research into the reasons why. Like so many conditions, allergies appear to be linked to both genetic and environmental factors, making isolation of the causes difficult. Meanwhile, parents are provided with copious amounts of advice, often inaccurate, not evidence-based or simply difficult to follow in order to deal with their children's allergic sensitivities and reactions. Today on Up Close, we speak to a paediatric gastroenterologist and allergist who is making substantial progress in exploring the real reasons behind the allergy explosion and how we should be responding to it. Providing clarity for parents and a better future for our kids. Professor Katie Allen is the Director of Population Health, Genes and Environment and group leader of Gastro and Food Allergy at the Murdoch Children's Research Institute and the Royal Children's Hospital. Welcome to Up Close, Katie. 

KATIE ALLEN
Hello. 

SHANE HUNTINGTON
Katie, what are the typical symptoms that you might see when a child is brought to the hospital with a food allergy reaction?

KATIE ALLEN
Well, we like to think of food allergy as comprising of a number of different conditions, but the one that most people are worried about is what we call IgE-mediated food allergy. So IgE-mediated food allergy means immunoglobulin E mediated food allergy. So immunoglobulin is one of the fighting antibodies in the body which we use to attack things that we don't really need to have. The reason parents are worried about this condition is it's the only one associated with the life-threatening condition anaphylaxis. So these children are ones that have, what we call, immediate reactions or acute reactions to a food very soon after they've eaten it. So usually within a few minutes, but up to within half an hour to an hour after eating the food. It typically occurs early in the life of the infant. So usually the first or second time the child's exposed to the food. So a very small dose of the food, a bite or a sip will result in what could be simply looking like they've been stung by an insect, they've had a bee sting. So their face may swell up, which we call angioedema, they may get welts all over their body, which we call hives or urticaria or generalised urticaria. They may vomit and some of them go on to get the most severe consequence which is called anaphylaxis. That is problems with breathing or wheezing, difficulties with their airways or they may collapse. 

SHANE HUNTINGTON
Katie, what is actually happening inside a child's body to cause these type of reactions?

KATIE ALLEN
So with adverse reactions to foods, there's lots of different types of reaction, but again, coming back to the IgE-mediated mechanism, there's a very clearly orchestrated mechanism of response. So the first time that the body will have seen the food that it's becoming allergic to, we say it becomes sensitised to the food and it mounts an antibody response which says, danger, this is not good. Then the next time that the body is exposed to that same food, it mounts an attack and the immune system attacks the foreign protein from the food that's been ingested and it does something that we call cross-links the IgE antibodies that reside on mast cells or basophils, which are particular allergic cells within the body. When those proteins are linked across the IgE antibodies, they cause what we call a degranulation process. So the mast cells or the basophiles are histamine-containing cells in our body. They're like little chemical bonds that live in different parts of our body and they explode and they release histamine. Most people know what histamine does to you, or let's put it the other way. Most people know what antihistamine does to you, because we all take antihistamine tablets for hay fever or different types of allergic reactions. So if someone has a histamine release, they get all those sorts of symptoms that I just described before. 

SHANE HUNTINGTON
Now, it seems to me as though our immune system is so very good at changing and adapting. Why is it that we get - or as children, caught in this loop, if you like, where our immune system reacts and it's life threatening, shouldn't our immune system adapt to these circumstances and then be able to handle these foods later down the track? 

KATIE ALLEN
Really, what you're asking is a very, very important question. Why does someone mount an allergic response? At the base of that question is, why is there an epidemic of allergy that is occurring? When you try to understand why we have an IgE system in the first place, it's there because it fights parasites in general. So that may be one of the hypotheses that we talk about why there seems to be a rise in allergic disorders, because the IgE system can fight parasites. So the argument is, if you have less parasites, then maybe you have a disregulated or overactive IgE immune system. That actual hypothesis is called the Old Friends Hypothesis, which is distinct and separate from the hygiene hypothesis, but probably, not too dissimilar in the mechanisms involved. 

SHANE HUNTINGTON
Now, certain foods are causing these problems. What is it specifically about these foods that alert us to react in this certain way? Is there something we know about peanuts, eggs, these sorts of things that cause this problem? 

KATIE ALLEN
So when we think about the most common types of food allergies in childhood, we talk about the big eight. They cause, in childhood, more than 90 per cent of IgE-mediated or immediate food reactions. That consists of cow's milk, soy, egg, wheat, fish, shellfish, tree nuts and peanuts. No one really knows why those foods versus other foods - other than to say it's the protein component for a start and then we do know that there are subcomponents for each of these different proteins. So for instance, with the peanut allergen, there are at least nine different subcomponents. They're called Ara h subcomponents, Ara h 1 to 9, and different people have different allergic responses to different subcomponents. People who are most likely to be severely allergic are more likely to have reactions to all or more than one or two subcomponents. There are families of allergens, and when I talk about allergens, they're the part of the protein that initiates and activates the immune response, but there are different families that we group together. So if you have an allergy to one type of tree nut, for instance, cashew, you're much more likely to also react to another sub-related protein family like pistachios. So cashew and pistachio are often co-locators, food allergic conditions. So there are families we call and things like the profilin superfamily where different types of foods come under groupings, but why the big eight or the important eight? We're not absolutely sure. What we do know is that there seems to be quite distinct regional and geographical differences so that some foods more commonly trigger food allergies in certain regions than in other areas. There's also cross-reactivity that varies across different regions. In Singapore for instance, there is something called bird's nest soup anaphylaxis which we don't have in Australia, but then we don't eat bird's nest soup in general. In Europe, for instance, the commonest cause of adult onset anaphylaxis in one of the more recent studies, the Europrevall study, appears to be celeriac or the celery root. The celery root has widespread use within the food chain supply in Switzerland, and so that is probably why there's a higher sensitisation rate. So when I say high sensitisation rate, I mean that the body is alert and has activated IgE antibodies to that particular protein. 

SHANE HUNTINGTON
If you look at something that is seen commonly around the entire world, like eggs, is there a distribution of allergic reactions in different countries that is disproportionate to population? 

KATIE ALLEN
As you say, cow's milk and egg are probably the two most common infant foods that are common to almost every culture. So they are the most common food allergies around the world in children. Adults, by the way, have a slightly different profile, and again, we don't know exactly why. Peanuts are widely eaten around different countries, but some countries like the Sub-Sahara Africa and places like India and Sri Lanka have a high peanut content in their diet and yet, they have a very low prevalence of peanut allergy. So it's probably a combination of the allergen itself, what's commonly in the diet and then the environmental factors which are probably the strongest factor that could be related to why some people get some food allergies and the others don't. One thing that is important to remember is, there are probably two distinct types of IgE-mediated food allergy and this isn't really discussed widely in the literature. It is a concept that is becoming more recognised, and that is that there are transient food allergies and then there are the more permanent food allergies. So for egg and cow's milk, most children will outgrow those food allergies in the first few years of life. It's thought that about 80 per cent of children will outgrow egg allergy in the first three to five years of life. Similarly, about 80 per cent will outgrow cow's milk allergy in the first one to three years of life. In contradistinction to that, peanut and tree nut allergy are both more likely to be lifelong with only about 20 per cent outgrowing those allergies by the age of 10. Now, that is being well described in literature and is an obvious clinical phenomenon since we see it in our patients in clinics. What isn't well characterised and described is why that might be, but there is an evolving hypothesis that the transient food allergies are likely to be transient, because they have what we call conformational versus linear epitopes. So if you take an epitope, which is the part of the protein that is important for the allergic reaction and twist it into a ball of wool, then that's confirmationally changed as opposed to it being a long piece of wool where it's in a linear form.  So egg proteins are in a confirmational epitope, so the protein's all curled up and it's recognised by the immune system in that way. Only about 20 per cent of children are allergic to both the confirmational epitope and the linear epitope. So what that means clinically, is that if you cook the food allergen in egg and destroy that confirmational 3D structure and make it into a linear epitope, the child can then tolerate the linear epitope. So they can therefore, still be allergic to raw and cooked egg, but then tolerant to egg in baked goods to small amounts of the linear epitope. 

SHANE HUNTINGTON
I'm Shane Huntington and you're listening to Up Close. In this episode, we're talking about food allergies in children with paediatric gastroenterologist and allergist, Professor Katie Allen. Katie, obviously, when a patient presents at the Children's Hospital, you know that there is a problem, but outside of that, how do you go about testing for these allergies in children? 

KATIE ALLEN
So you've touched on how patients present to hospitals and it's one of the things I commonly talk to families and give talks about this content. That is that it doesn't take a rocket scientist to work out that there's something that's going wrong. The mother says, I've given the food to my child, they've blown up like a balloon. I think it's the food they've just eaten. It's very easy to distinguish that it looks like an allergic reaction to the parents and it's easy to confirm when they come in with a history. What we then go on to do is to confirm, firstly, the history, then we'll test them for what we call this immunoglobulin-E or IgE antibody with either a skin prick test or a blood test. Now, what that does is it confirms that the mechanism of the reaction is IgE-mediated, but if there's either a doubt about the history or the level of antibody they're making, we may go on to do what we call the Gold Standard, which is an oral food challenge where we actually give the food to the child. 

SHANE HUNTINGTON
In cases where you do find food allergies, are those children more likely to have other allergies as well? Like allergies of the skin and so forth? 

KATIE ALLEN
Yeah. So food allergy is well-recognised and we ourselves have polished this data. It's well-recognised to be associated with eczema which is a skin allergy and it's thought to be - but hasn't yet been well-characterised to be part of what we call the atopic or allergic march. That's where we think that children who have early onset eczema and food allergy go on to develop other allergic conditions, including allergic rhinitis and allergic forms of asthma. 

SHANE HUNTINGTON
In the case where you have a young child, a baby, is it best to simply keep that child away from these particular foods? Is that the approach the parents should be taking?

KATIE ALLEN
That is the approach from five years ago and it has turned on its head 180 degrees. So patients who have been under my care for 10 years are often saying, wow, things have changed in the last three to five years and it has been as recent as that. In the past, it was thought that if we avoided giving these children foods that can make them allergic, then we may prevent them from ever developing an allergy to that food. So maybe their immune system was too sensitive, too young and too immature. So let's not give them that food. There's now, quite strong, emerging evidence that that is not being protective. So it's not preventing the rise in rates of food allergy. It does not appear to prevent children from getting the food allergy. So what we say now, is that to introduce allergenic foods between four and six months or around the age of six months is safe, that is, it won't increase the rates of allergy and it may even be protective. So we've gone even further to say that introduction of solids around the age of six months may even protect you from getting food allergies. 

SHANE HUNTINGTON
Do we have some data on the impact that that has in terms of how much less likely children would be to develop allergies as a result to early introduction? 

KATIE ALLEN
So there are now, probably four human-based papers or clinical papers that have looked at various, different types of food and the prevention of a particular type of food allergy. One of those papers is our own paper, the Koplin paper and that has been published in 2011 and has described that children who introduce cooked egg between the ages of four to six months are five times less likely to get egg allergy than if they introduce it after what was the currently recommended age of 10 months.

SHANE HUNTINGTON
Now, this must be a source of great trepidation for a lot of parents. We're talking about four-month-old babies. Is it advisable to do this while you're parked out the front of a medical facility? We're talking about potentially severe reactions. How do they go about this? 

KATIE ALLEN
Well, the first thing is that in our health nut study, which we've published already in a number of papers from one you mentioned earlier in your brief is that parents would come to us and say, thank goodness we're having this study, because we were planning to park in the car park of the children's hospital to give our first peanut butter sandwich. I would have heard that a dozen times at least. Obviously, that's not scientific evidence, but it's pretty reasonable evidence that community is quite concerned. The Australian Society of Clinical Immunology and Allergy Guidelines have been informed by the recent evidence and the UK, Europe and US guidelines have also now changed to reflect that there is no reason to avoid the food and that may even be protective to introduce it. We say four to six months in our ASCIA guidelines, but the problem with the current guidelines is they're now in contravention to the WHO and National Health and Medical Research Council Guidelines. Now, these latter guidelines, the NHMRC guidelines are currently under review and my understanding is they are going to come to a compromised position where we say around the age of six months, it's safe to give these foods. So with regards to the trepidation, however, we always say, start with a tiny dose. It's likely to be safe, people still can get egg allergy, but the reactions are likely to be milder when they're young anyway. So there's some pretty reasonable evidence that the reactions in infants are smaller and milder than in the reactions in older children anyway. So in order to be diagnosed with a food allergy, you need to have had a reaction, whether it's at home with a tiny amount or in a formal food challenge with a doctor close by, but for all intents and purposes, it is a fairly safe way to do it, is to give a tiny dose at home. Increase that dose slightly as you do for all foods. 

SHANE HUNTINGTON
Now, some children who have these sorts of reactions will get, essentially, burns on their skin in addition to it being a problem if they ingest it. Does a skin reaction guarantee an oral reaction or vice versa? 

KATIE ALLEN
No. That's a very interesting point. We don't like to use the word, burns, because that has connotations that it's quite dangerous. If you touch a food, it's similar to giving a child a skin prick test. That's how we do the skin prick test. We put a little drop of the allergen or the food in a commercial form, we put it onto the child's skin and then we introduce it into the dermis by just a little scratch. That then causes a real reaction, because the histamine cells that are in the epidermis react and release histamine and other mediators of the allergic reaction. So the contact reaction that you're talking about is usually local and self-limited. So often, somewhat jokingly say you can't really sit on a banana and get a banana allergy, you have to eat it. So there are some people who will have a contact reaction that can safely eat the food, because just like about 50 per cent who have children who have a positive skin prick test can safely eat the food. So a skin prick test or a contact reaction is only right about half of the time. So the only exception to the rule of that is contact to the lip and that probably does predict, because it's part of the oral and the GI tract. 

SHANE HUNTINGTON
How does the timing of the introduction of these foods relate to how long mothers today are encouraged to breast feed? 

KATIE ALLEN
Again, you touch on a highly controversial point and that is that the World Health Organisation and WHO guidelines recommend exclusive breastfeeding for the first six months of life. Now, that's for clear and obvious reasons, particularly in developing countries where the water supply is not as secure and babies can literally die from having formula from having contaminated water supplies. In Australia, we still need to encourage exclusive breast feeding for a whole raft of reasons. Probably, it's good to prevent infection, it may have an impact on intelligence and IQ. There isn't any evidence that it's protective for allergic disease and in fact, it looks like most of the cohort studies now show that people who breastfeed longer are seen to be more likely to have the risk of allergy. Now, it's just an association that's spurious, because those who breastfeed longer are the food allergic in family history families. So they're breastfeeding longer, because they think they should and that's not being protective, nor is it being problematic. So then we come up with, well, what do we do with these recommendations that the allergic societies are recommending? The way we get around that is to say, well, breastfeed and introduce solids around the age of six months and hopefully, everyone will be reasonably comfortable with that. 

SHANE HUNTINGTON
I'm Shane Huntington and my guest today is paediatric gastroenterologist and allergist, Professor Katie Allen. We're talking about food allergies in children here on Up Close. Katie, your work has looked at other environmental factors involved in increasing the risk of developing allergies. What are these? 

KATIE ALLEN
There are two other major areas of endeavour, and that includes the hygiene hypothesis or the old friend's hypothesis and the other factor is vitamin D and sunlight exposure. 

SHANE HUNTINGTON
Can you tell us, how is the introduction of vitamin D or the amount of vitamin D that the child ingests related to this food allergy onset? 

KATIE ALLEN
So there's now evidence - and again, we've contributed to this data that the further from the equator that the child resides, the more likely they are to have an egg and peanut allergy. That's being shown both in the Southern Hemisphere by ourselves, but also, in the Northern Hemisphere in the US. That is after adjusting for the fact that they're in large population centres, they're more likely to be allergic doctors, therefore, people are more likely to access them. So we think it is a definite effect and it's this ecological data that makes us consider that UV exposure, which has an impact on vitamin D, may be an important factor in the development of a robust immune system and prevention of allergic disease. There is some encouraging emerging data that we're producing ourselves, which is looking at the vitamin D story. It's hopefully going to be released very soon.

SHANE HUNTINGTON
Can you explain further the hygiene hypothesis? This is something many of our listeners will have heard over many years now and for a while, it was probably one of those areas that was more of a myth and a research tool, but it's gaining momentum. 

KATIE ALLEN
So the Hygiene Hypothesis gets defined by different people in different ways in different studies and by different experts. So I think the definition is a little bit difficult to define. In the first instance, it was described by Strachan in the UK. When he found a protection against allergic rhinitis in the '80s, the more children that you had, and he coined the phrase the Hygiene Hypothesis to describe the sibling protective effect. The idea has taken hold and seems to be holding up to a whole lot of other research about allergic disease, in general, and it has been applied to the food allergy epidemic and there are certainly strong, emerging evidence. Some of the evidence we've produced - again, published in the Koplin paper in 2012, which shows that the number of siblings that you have and pet exposure, particularly dog exposure is protective against the development of egg allergy and food allergy in general. Again, it's a step away from having direct evidence, but the idea is the more siblings you have, then the more exposure you have to childhood infections. If you have a pet, particularly a dog, then you're exposed to endotoxins and other bacteria in that dog's mouth. Perhaps in not such a nice way to imagine, but we share organisms across species and that probably helps to stimulate the immune system. If you take the Hygiene Hypothesis in the correct direction, we think it's probably mediated through microbial diversity in the intestine. There's been a recent 2012 publication of the faecal microbiome of the body and it was published in Nature quite recently and it makes for fascinating reading if you're a gastroenterologist. Perhaps less so if you're not, but the diversity of species that we carry on our skin, underneath our gum near our teeth, in various parts of our body are quite amazingly diverse. There is quite a lot of interest in the fact that 90 per cent of the cells that we carry are actually bacterial cells. The rest of our cells or our body cells are only 10 per cent. So there's this great unknown about the microbial diversity, particularly in our gut. There is some evidence, for instance, that breastfed babies have more microbial diversity than bottle-fed babies. So when Mum says you are what you eat, she's really, pretty right. You are also microbially diverse with what you eat. So that's possibly why allergen exposure is probably a good thing as well, because we're also feeding our bugs when we eat food. 

SHANE HUNTINGTON
Now, this is in stark contrast to what most parents would come across. If they ever turn on the television, they'll see all these advertisements telling them the bacteria of any type in the home is bad. How do we encourage parents to essentially allow that exposure? Or is it just through that relaxation of a second child, you're less concerned about such things that we get these great results? 

KATIE ALLEN
You have to be aware that none of these studies have gone and done studies at the individual household level. Most of these studies are looking at the more general population level and so, when we look at the changes that have occurred across the whole population in the last 20, 30 years. In fact, the fact is that we think are causing the rise in food allergy have to be environmental, because we know that our genes can't have changed that quickly and we also know that the problem is occurring mostly in developed countries and is rising in developing countries, we ourselves have published and worked.In china, for instance, there seems to be an emerging epidemic occurring there as well. So we know it's something to do with modern lifestyle. As a city becomes more urbanised, the risks go up and that's only indirect evidence that we think it's to do with the general exposures that the community gets to farm animals to pets and sibling size, number. All those sorts of things change when you urbanise a city. We're not talking about the individual hand-wipe level of how clean an individual house is. We do know at the general level that developed countries versus developing countries, there is a cleaner water supply. The food chain supply is cleaner. There's more widespread use of antibiotics. So my belief is at the generation population level. Not at the individual household effect level. 

SHANE HUNTINGTON
Katie, we've discussed a lot of the reasons behind these allergies becoming so prolific amongst our children. What about the cures?

KATIE ALLEN
That's the $64 million question, really. There is some really exciting research that's going on now, which is looking to induce tolerance in children who already have food allergy. The most encouraging results have come from what we talked about before, the food allergy that is transient. I think why they're more likely to be effective is that if a child's body has naturally got a high chance of outgrowing the food allergy, then maybe we can hasten the development of tolerance. So there's already a potential mechanism that we just need to activate. The more resistant conditions, I think, will be the peanut and tree nut allergies, but again, there's some encouraging results that are coming to hand. Now, those areas include all immunotherapy trials where the child is given minute amounts of the allergen, or the peanut or the egg and that is given in a commercial form and it's given in a very careful, gradated way over a long period of time under medical supervision. So we don't suggest people try that at home. If you are allergic, you should continue to avoid that food as a form of management.Then the second type of treatments that are on the horizon are vaccines and peptide immunotherapy, where we give injections of small amounts of the peptide to try to trick the immune system to become intolerant. There's some other sorts of trials that are under way which shows some great promise, including a new Chinese herbal formulation that's under development in the US. So everyone's keen to try and find a solution, because certainly, in Australia, our waiting lists are overwhelmed.

SHANE HUNTINGTON
We have entered the century of the genome, essentially, and we're also in this space of moving towards personalised medicine. Are we a long way from being able to look at an individual's genome and specifically treating them for their allergies? 

KATIE ALLEN
I think that is a very exciting area, but possibly, as is often the case in these new technologies, not in the way we imagine here in 2012. We actually have a study that's just been completed and is being analysed where we look at all our food allergic cases and our food tolerant cases as controls. I don't expect that we'll find one gene cause a food allergy, because as I said before, the food allergy epidemic is a new epidemic. If there was a genetic cause, it would have been around for millennia. So it has to be a gene-environment interaction. There may be a genetic predisposition, but we know that is has to be something to do with an environmental factor. Where I think the big movement forward will come from genetic technology is stratifying risk by genetic predisposition so that there may be some people who have a more sensitive genetic predisposition that makes them more likely to do poorly to that environmental risk factor. I often give this as an example to people when I'm trying to explain an epidemiological concept, because whenever I talk about - we think pets may be protective or we think that exposures are important, they say, well, that didn't happen in my case. Then I say, well, we know that lung cancer is caused by smoking, but some people smoke and don't get lung cancer and some people get lung cancer who never smoked. So the reason why some people have a bad outcome and some do may be genetically-based. So again, with food allergy, I think there are people who are more genetically at risk than other people. I think there are some population-environmental factors that will be across the whole population and there are some factors that will be more specific for those who are genetically at risk. So we have actually found one of those first factors and that is the filaggrin gene. The filaggrin gene is a gene that predicts for an increased risk of having eczema, and we know from our findings that if you have the filaggrin gene, you're twice as likely to get eczema, but you're also much more likely to be sensitised to a food. So you're more likely to be in the alert and aware state in the first year of life. That gene does not predict for the development of food allergy. That's the second step. So you have a genetic predisposition, you're more likely to be food sensitised. If you're food sensitised, there's probably another factor that makes your body become allergic or become tolerant. So as I said before, in skin prick test positive cases, only about half are allergic and the other half are tolerant. We think that second factor is to do with microbial diversity and vitamin D and allergen exposure. So more to do with the gut factors, while we think that genetic predisposition sets you up for the risk, we think there's a gene environment two-step hypothesis as there are for a lot of diseases of multiple causes. 

SHANE HUNTINGTON
Katie, just finally, when we look at the number of kids presenting with these problems and it has been increasing over decades and yourself, referred to it as an epidemic. Are we reaching saturation point, or are the numbers telling us that this is just going to keep getting worse? 

KATIE ALLEN
It is impossible to predict. When we say epidemic, to be clear, what we can say is prevalence rates that we reported here in Melbourne, Australia with one in 10 infants having challenged, proved a food allergy were higher than predicted, but we have never formally challenged every child who has a positive skin prick test in a population sample of this size anywhere in the world before. So we can't say we've measured it correctly before, so what we say is it's higher than predicted. It's likely to be rising, but then you look, even just at reports of our waiting lists going through the roof and you speak to parents, and they say, I've never seen this before. We know it's a new set of condition and the prevalence of that condition is at a high level. What we also know is that the rates of anaphylaxis are rising, and that's a fairly objective factor and that's being recorded in a number of different reports around the developed world now. It's been about a five to seven-fold increase over about a 10-year period of time. So from the mid '90s to the mid-2000s and we've also seen a rise in positive skin prick test, positive prevalence rates as well. So we think it is a rise. Whether we're halfway through, whether we're plateaued, only time will tell. My hope is, actually, that we don't really need to wait to find out, because the fact is that we predict the rise in food allergy, we will be able to reverse the trend by implementing changes to public health guidelines and therefore, my prediction is it will at least plateau. I'm hoping it may actually go away. That would be great as an outcome. 

SHANE HUNTINGTON
Professor Katie Allen, Director of Population Health, Genes and Environment and group leader, Gastro and Food Allergy at the Murdoch Children's Research Institute and the Royal Children's Hospital. Thank you for being our guest today on Up Close and talking about food allergies and children.

KATIE ALLEN
Thank you, Shane. 

SHANE HUNTINGTON
Relevant links, a full transcript and more info on this episode can be found at our website at upclose.unimelb.edu.au. Up Close is a production of the University of Melbourne, Australia. This episode was recorded on 13 November, 2012. Our producers for this episode were Kelvin Param and Eric van Bemmel. Associate Producer, Dyani Lewis. Audio engineer, Gavin Nebauer. Up Close is created by Eric van Bemmel and Kelvin Param. I'm Shane Huntington, until next time, goodbye.

VOICEOVER
You've been listening to Up Close. We're also on Twitter and Facebook. For more info visit upclose.unimelb.edu.au. Copyright 2012. The University of Melbourne.

 

 


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